J. Tushir-Singh (@tushirsingh_lab) 's Twitter Profile
J. Tushir-Singh

@tushirsingh_lab

Associate Professor @ucdavis,
Protein Engineering & Cancer Immunotherapy
“The harder you work, the better you will do”: Vince Lombardi
Scientist and Farmer

ID: 837494714274304000

linkhttps://thesinghlab.org/ calendar_today03-03-2017 02:47:54

374 Tweet

183 Followers

104 Following

J. Tushir-Singh (@tushirsingh_lab) 's Twitter Profile Photo

Our New paper describe the crucial regulatory epitope for FAS agonist antibodies but also adds to the FAS/CD95 CAR-T Bystander tumor killing function. Stay tuned for our follow up work on disruptive new science to target Fas differently in T-cell vs tumors nature.com/articles/s4141…

NEJM (@nejm) 's Twitter Profile Photo

#ESMO23: Tarlatamab, a bispecific T-cell engager targeting DLL3 and CD3, led to an objective response in 40% of patients, with 68% alive at 9 months. Cytokine-release syndrome, mainly of low severity, occurred in 51%. Full DeLLphi-301 trial: nej.md/3QpVz27

#ESMO23: 

Tarlatamab, a bispecific T-cell engager targeting DLL3 and CD3, led to an objective response in 40% of patients, with 68% alive at 9 months. Cytokine-release syndrome, mainly of low severity, occurred in 51%. 

Full DeLLphi-301 trial: nej.md/3QpVz27
Cancer Research Institute (@cancerresearch) 's Twitter Profile Photo

In a new study, UC Davis Health researchers identified a crucial epitope on the CD95 receptor that can cause cells to die. This new ability to trigger programmed cell death could open the door for improved cancer treatments. More: bit.ly/3FsyoxE #CART #CancerResearch

UC Davis Health (@ucdavishealth) 's Twitter Profile Photo

A team led by Jogender Tushir-Singh identified a crucial mechanism on a specific cell receptor that can cause cells to self-destruct. This ability to activate the receptor — Fas — and trigger cell death, could open the door for improved cancer treatments: ucdavis.health/494aLsV

L. Fernando Santana 🇵🇷 (@lfsantana68) 's Twitter Profile Photo

Read our latest paper rdcu.be/dq5Bj on how the degree of Kv2.1 clustering drives sex-specific differences in Cav1.2 channel clustering and function. Published with Springer Nature in Communications Biology! A collab with @JimTrimmer01 and @clancyatheart labs from UC Davis Physiology!

UC Davis Health Medical Microbiology & Immunology (@ucd_mmi) 's Twitter Profile Photo

Our department is proud to be ranked #17 for NIH funding in the field of Medical Microbiology and Immunology for all medical schools in the country.

Dmitriy Zamarin MD PhD (@dmitriyzamarin) 's Twitter Profile Photo

Love ovarian cancer? Hate ovarian cancer? You’re not alone! Submit your abstracts to the Biennial Rivkin-AACR Ovarian Cancer Research symposium! This will be a fantastic meeting with the latest and greatest in ovarian cancer research. myemail-api.constantcontact.com/Abstracts-due-…

L. Fernando Santana 🇵🇷 (@lfsantana68) 's Twitter Profile Photo

Check out our new collaboration with Rose Dixon from UC Davis Physiology in pnas (pnas.org/doi/10.1073/pn…). We observed two modalities of beat-to-beat ATP fluctuations in ventricular myocytes based on SR-mitochondrial coupling strength. (1/2)

J. Tushir-Singh (@tushirsingh_lab) 's Twitter Profile Photo

*NEW Paper ALERT* Our new work in Nature Communications on FasL-mediated cancer cell death regulation has revealed that evolutionary substitutions (humans vs. primates) in the FasL extracellular domain render human FasL differentially susceptible to plasmin protease cleavage, a key

ilyas sahin, MD (@ilyassahinmd) 's Twitter Profile Photo

Humans are more cancer-prone than primates despite over 98% genomic similarity. A FasL mutation unique to humans allows plasmin in solid tumors to weaken immune attack Nature Communications * . Could blocking it boost immunotherapy?

Humans are more cancer-prone than primates despite over 98% genomic similarity.  A FasL mutation unique to humans allows plasmin in solid tumors to weaken immune attack <a href="/NatureComms/">Nature Communications</a> * . 
Could blocking it boost immunotherapy?
Medical Xpress (@medical_xpress) 's Twitter Profile Photo

A gene therapy targeting X chromosome silencing has shown potential to reactivate healthy MECP2 genes in #RettSyndrome models, improving symptoms and offering hope for X-linked disorders. Nature Communications doi.org/g9tww8 medicalxpress.com/news/2025-07-c…